Results of experiments utilizing several different approaches strongly suggest that dengue virus-antibody comples infct monocytes from the peripheral blood of non-immune humans and monkeys. Cells of the lymphocyte series did not support virus replication. The functional age of the sub-population of monocytes capable of infection with dengue virus-antibody complexes is being investigated using cytochemical stains. The dynamics of dengue virus infection of monocytes in vitro is being studied, particularly with reference to the morphological relationships between virus and cellular structures. Stains for lysosomal enzymes and for dengue antigen are being used to determine the precise relationship of dengue antigen to lysosomes. In the dengue shock syndrome, complement activation proceeds via both classical and alternate pathways. If dengue virus infection of monocytes could directly generate complement activation, this might explain the findings in primary infection dengue shock syndrome in infants. The occurrence of C3 proactivator conversion activity is being sought in cultures of human monocytes infected with D2 virus. Since the kinetics of human dengue infection suggests that vascular permeability factors responsible for shock are released only during the phase of active immune elimination of dengue infected cells, the release of nnflammation mediators from dengue infected monocytes upon destruction is being studied.